Continued studies of experimental allergic encephalomyelitis (EAE) induced in laboratory animals will define (1) the relative importance of cerebrovascular permeability and transport of sensitized lymphoid cells (LC) and antibodies into the neuraxis of Lewis rats as pathogenetic determinants of EAE, utilizing isotopic labelled (I131 and I125) normal and immune rat gamma-globulins, (2) the significance of perivascular fibrin deposition and its relationship to other clinical and histopathologic hallmarks of EAE, (3) the conditions for cellular transfer of EAE in Lewis rats with sensitized LC, including the role of a sub-cellular component demonstrable in LC supernatants, and (4) role of acute and chronic measles encephalitis of hamsters on their susceptibility to EAE and the EAE-inducing activity of hamster nervous tissue.